DISTINCTIVE FUNCTIONS OF SYK AND LYN IN MEDIATING OSMOTIC STRESS-INDUCED AND ULTRAVIOLET-C IRRADIATION-INDUCED APOPTOSIS IN CHICKEN B-CELLS

By taking advantage of the established chicken B cell line, DT40 cells , which do not express tyrosine kinase Syk or Lyn, functional soles or Syk and kyn in apoptotic response elicited by cellular stress were in vestigated, DT40 cells underwent apoptosis after hyperosmostic stress, In Syk-deficient DT40 cells, this apoptotic process was significantly enhanced, Ectopic expression of wild type, but not kinase-inactive, p orcine Syk in Syk-deficient cells rescued cells from osmotic stress-in duced apoptosis, demonstrating that the presence of functionally activ e? Syk is necessary to protect cells from osmotic stress-induced apopt osis. In comparison these was no effect on osmotic stress-induced apop tosis in Lyn-deficency DT40 cells, Interestingly, while Syk, was not i nvolved in ultraviolet C (UVC)-induced apoptosis, a a deficiency of Ly n rendered cells resistant to UVC irradiation, These observations defi ned Syk and Lyn as important mediators of apoptosis in DT40 cells in r esponse to osmotic stress and UVC irradiation, respectively, Furthermo re, osmotic stress, but not UVC irradiation, could activate c-Jun N-te rminal kinase (JNK) in DT40 cells. A deficiency in either Syk or Lyn d id not affect the osmotic stress-induced activation of JNK. Wet theref ore, concluded that Syk and Lyn regulate the apoptotic responses to os motic stress and UVC irradiation independently of the JNK pathway in D T40 cells.